INTRODUCTION Intensive care units have come to represent the most frequently identifiable source of nosocomial infections within the hospital, with the infection rates and rate of antimicrobial resistance several fold greater than the general hospital settings. Ventilator-associated pneumonia (VAP) is defined as nosocomial pneumonia in mechanically ventilated patients that develops more than 48 hours after initiation of mechanical ventilation (MV). VAP is the second most common nosocomial infection after urinary tract infection in pediatric intensive care unit patients accounting for 20% of nosocomial infection in this population (1). Langer and co-workers divided VAP into early onset VAP which occurs within 5 days of mechanical ventilation and late onset VAP, which develops five or more days after initiation of mechanical ventilation. (2) The importance of segregating VAP into early and late is that, the pathogenesis, microorganisms responsible and outcome in these two groups are different and so the therapeutic implications also differ. Early onset VAP results from aspiration of endogenous community acquired organisms e.g. S. pneumoniae, H. influenzae, and other organisms (aerobic gram negative bacilli). Late onset VAP is more severe and results usually from aspiration of gastric/oropharyngeal secretions and caused by potentially drug resistant organisms like methicillin resistant staphylococcus aureus (MRSA) and Pseudomonas. The diagnosis of VAP is made by clinical criteria recently revised by National Nosocomial infection Surveillance System (NNIS) for pediatric patients (3). It should be however noted that a “gold standard” for microbiological diagnosis of VAP does not exist. For microbiological diagnosis either bronchoscopic methods like bronchoalveolar lavage, protected specimen brushing (PSB) or non-bronchoscopic methods like quantitative endotracheal aspirate (ETA) is used in most intensive care units (ICUs).